N⁶-Methyladenosine in Vascular Aging and Related Diseases: Clinical Perspectives

Aging and Disease, Journal Year: 2023, Volume and Issue: unknown, P. 0 - 0

Published: Jan. 1, 2023

Aging leads to progressive deterioration of the structure and function arteries, which eventually contributes development vascular aging-related diseases. N⁶-methyladenosine (m⁶A) is most prevalent modification in eukaryotic RNAs. This reversible m⁶A RNA dynamically regulated by writers, erasers, readers, playing a critical role various physiological pathological conditions affecting almost all stages life cycle. Recent studies have highlighted involvement aging related diseases, shedding light on its potential clinical significance. In this paper, we comprehensively discuss current understanding implications. We molecular insights into association with realities, emphasizing significance unraveling mechanisms underlying aging. Furthermore, explore possibility regulators as indicators for early diagnosis prognosis prediction investigate therapeutic m⁶A-associated anti-aging approaches. also examine challenges future directions field highlight necessity integrating knowledge patient-centered care. Finally, emphasize need multidisciplinary collaboration advance research application.

Language: Английский

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A review on the role of RNA methylation in aging-related diseases

International Journal of Biological Macromolecules, Journal Year: 2023, Volume and Issue: 254, P. 127769 - 127769

Published: Oct. 30, 2023

Language: Английский

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m6A-modified circCacna1c regulates necroptosis and ischemic myocardial injury by inhibiting Hnrnpf entry into the nucleus

Cellular & Molecular Biology Letters, Journal Year: 2024, Volume and Issue: 29(1)

Published: Nov. 12, 2024

Abstract Background Circular RNAs (circRNAs) are differentially expressed in various cardiovascular diseases, including myocardial infarction (MI) injury. However, their functional role necroptosis-induced loss of cardiomyocytes remains unclear. We identified a cardiac necroptosis-associated circRNA transcribed from the Cacna1c gene (circCacna1c) to investigate involvement circRNAs cardiomyocyte necroptosis. Methods To circCacna1c during oxidative stress, H9c2 cells and neonatal rat were treated with hydrogen peroxide (H 2 O ) induce reactive oxygen species (ROS)-induced death. The N 6 -methyladenosine (m A) modification level was determined by methylated RNA immunoprecipitation quantitative polymerase chain reaction (MeRIP–qPCR) analysis. Additionally, an pull-down assay performed identify interacting proteins cardiomyocytes, regulatory target protein expression tested using western blotting assay. Furthermore, MI mouse model constructed analyze effect on heart function Results found be reduced exposed stress hearts injured MI. Overexpression inhibited necroptosis induced injury, resulting significant reduction size improved function. Mechanistically, directly interacts heterogeneous nuclear ribonucleoprotein F (Hnrnpf) cytoplasm, preventing its translocation leading Hnrnpf levels within nucleus. This subsequently suppresses Hnrnpf-dependent receptor-interacting kinase 1 (RIPK1) expression. fat mass obesity-associated (FTO) mediates demethylation m A necrosis facilitates degradation circCacna1c. Conclusion Our study demonstrates that can improve following MI-induced injury inhibiting Hnrnpf/RIPK1-mediated Therefore, FTO/circCacna1c/Hnrnpf/RIPK1 axis holds great potential as effective for attenuating caused ischemic disease. Graphical

Language: Английский

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Targeting Epigenetic Regulation of Cardiomyocytes through Development for Therapeutic Cardiac Regeneration after Heart Failure

International Journal of Molecular Sciences, Journal Year: 2022, Volume and Issue: 23(19), P. 11878 - 11878

Published: Oct. 6, 2022

Cardiovascular diseases are the leading cause of death globally, with no cure currently. Therefore, there is a dire need to further understand mechanisms that arise during heart failure. Notoriously, adult mammalian has very limited ability regenerate its functional cardiac cells, cardiomyocytes, after injury. However, neonatal window regeneration allows for repair and renewal cardiomyocytes This specific timeline been interest in field cardiovascular regenerative biology as potential target cardiomyocyte repair. Recently, many have associated epigenetic regulation within heart. review summarizes current most promising regeneration, emphasis on targeting these models

Language: Английский

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An overview of the effects and mechanisms of m6 A methylation on innate immune cells in sepsis

Frontiers in Immunology, Journal Year: 2022, Volume and Issue: 13

Published: Nov. 24, 2022

Sepsis is a severe clinical syndrome caused by dysregulated systemic inflammatory responses to infection. Methylation modification, as crucial mechanism of RNA functional can manipulate the immunophenotype and activity immune cells participate in sepsis progression. This study aims explore N6-methyladenosine (m6A) methylation modification cell-mediated through keyword search.Literature retrieval.Literature retrieval reveals that m6A implicated sepsis-induced lung injury myocardial injury,as well sepsis-related encephalopathy. Furthermore, it found regulate inhibiting chemotaxis neutrophils formation neutrophil extracellular traps suppressing macrophage phagocytosis, thereby playing role sepsis.

Language: Английский

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